Fig. 7
Overexpressing miR-26a in GSCs enhances angiogenesis in vivo. a the number of branches of blood vessels (5 mm) around the CAM vehicle; b transplanted tumors in nude mice; c tumor volume and weight; d VEGF level in the serum of nude mice measured by ELISA; e protein levels of PTEN and VEGF measured by Western blot analysis; f CD31-MVD detected by immunohistochemistry (× 400); *, p < 0.05, compared with the GSCagomir-NC group; #, p < 0.05, compared with the GSCantagomir-NC group; all data were expressed as mean ± standard deviation; comparisons between two groups were analyzed using unpaired t-test; comparisons among multiple groups were analyzed by the one-way ANOVA; the experiment was repeated three times; ANOVA, analysis of variance; miR-26a, microRNA-26a; NC, negative control; PTEN, phosphatase and tensin homolog deleted on chromosome ten; Akt, protein kinase B; VEGF, vascular endothelial growth factor; GSCs, glioma stem cells; CAM, chorioallantoic membrane; MVD, microvessel density; ELISA, enzyme-linked immunosorbent assay; GSCagomir-NC, agomir-NC-transfected GSCs; GSCantagomir-NC, antagomir-NC-transfected GSCs; GSCmiR-26a agomir, miR-26a agomir-transfected GSCs; GSCmiR-26a antagomir, miR-26a antagomir-transfected GSCs